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Published on: June 18, 2020
Increased plasma endothelin-1 levels in patients with cirrhosis and esophageal varices
1Third Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Insights
Plasma endothelin-1 levels were higher in cirrhosis patients with esophageal varices. This may be a compensatory mechanism for vasodilation in liver cirrhosis and portal hypertension.
Area of Science:
- Cardiovascular Physiology
- Hepatology
Background:
- Liver cirrhosis is associated with systemic vasodilation.
- Endothelin-1 is a potent vasoconstrictor peptide with implications in cardiovascular regulation.
Purpose of the Study:
- To measure plasma endothelin-1 levels in patients with cirrhosis.
- To correlate endothelin-1 levels with clinical parameters and esophageal varices.
Main Methods:
- Plasma endothelin-1 levels were measured in 20 cirrhosis patients and 6 healthy controls.
- Correlations were performed with clinical data, laboratory parameters, and presence of esophageal varices.
Main Results:
- A trend towards increased endothelin-1 in cirrhosis patients was observed (6.0 +/- 2.5 vs. 4.4 +/- 1.5 pg/ml).
- Plasma endothelin-1 levels were significantly elevated in cirrhotic patients with esophageal varices (7.5 +/- 2.5 vs. 4.5 +/- 1.6, p < 0.05).
- Ascites, serum albumin, bilirubin, and prothrombin time did not significantly correlate with endothelin-1 levels.
Conclusions:
- Elevated endothelin-1 in cirrhotic patients with varices may be a compensatory response to systemic vasodilation.
- Endothelin-1 warrants further investigation as a potential biomarker in liver cirrhosis and portal hypertension.
Abstract:
We measured plasma levels of endothelin-1, a potent vasoconstrictor peptide, in 6 healthy controls and 20 patients with cirrhosis and correlated them with various clinical and laboratory parameters and other vasoactive substances. There was a trend toward increased endothelin-1 levels in patients with cirrhosis compared with controls (6.0 +/- 2.5 vs. 4.4 +/- 1.5 pg/ml, NS). The presence of ascites did not influence plasma endothelin-1 levels, and plasma endothelin-1 levels were not significantly correlated with serum albumin, serum bilirubin, or prothrombin time. Plasma endothelin-1 levels were significantly elevated in cirrhotic patients with esophageal varices compared with those without varices (7.5 +/- 2.5 vs. 4.5 +/- 1.6, p < 0.05). The elevation of endothelin-1 levels in patients with varices may represent a physiological compensation for the systemic vasodilation present in patients with liver cirrhosis and portal hypertension.
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